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目的检测apoE基因缺陷小鼠肝脏CuZnSOD基因CpG岛甲基化状态,探讨其与动脉粥样硬化发生发展的关系以及在动脉粥样硬化早期基因诊断中的意义。方法ApoE基因缺陷小鼠是用来建立动脉粥样硬化的成熟模型,本实验将18例7周龄apoE基因缺陷雄性小鼠及作为对照的18例7周龄正常的C57BL/6J雄性小鼠分别随机分成三组,在饲养至0周、7周、14周时取其肝脏,运用甲基化特异性PCR(methylation-specific PCR,MSP)法检测肝脏CuZnSOD基因CpG岛甲基化情况。结果不同时间段apoE基因缺陷小鼠与正常的C57BL/6J小鼠CuZnSOD基因CpG岛甲基化差异无统计学意义。结论apoE基因缺陷小鼠肝脏没有发生CuZnSOD基因启动子区CpG岛的异常甲基化,可能CuZnSOD基因启动子区CpG岛的异常甲基化没有参与动脉粥样硬化的发生发展。
Objective To detect the methylation status of CpG island of CuZnSOD gene in liver of apoE-deficient mice and to explore its relationship with the occurrence and development of atherosclerosis and its significance in the early gene diagnosis of atherosclerosis. Methods ApoE gene-deficient mice were used to establish atherosclerotic mature model. In this study, 18 male 7-week-old apoE-deficient mice and 18 normal 7-week-old C57BL / 6J male mice as controls The rats were randomly divided into three groups. The livers were harvested at 0, 7 and 14 weeks. Methylation-specific PCR (MSP) was used to detect CpG island methylation in the liver of CuZnSOD. Results The CpG island methylation of CuZnSOD gene in apoE gene-deficient mice and normal C57BL / 6J mice at different time points was not statistically different. Conclusion Aberrant methylation of CpG island in promoter region of CuZnSOD gene did not occur in apoE gene-deficient mice. It is possible that aberrant methylation of CpG island in promoter region of CuZnSOD gene is not involved in the development of atherosclerosis.